N E J West

B VH-IVUS findings predict major adverse cardiovascular events. The Viva Study (virtual histology intravascular ultrasound in vulnerable atherosclerosis)

Background Identification of high-risk atherosclerotic plaques offers opportunities for risk stratification and targeted intensive treatment of patients with coronary artery disease. Virtual Histology intravascular ultrasound (VH-IVUS) has been validated in human atherectomy and post-mortem studies and can classify plaques into presumed high- and low-risk groups. However, VH-IVUS-defined plaques have not been shown to be associated with major adverse cardiovascular events (MACE), or biomarkers that confer increased cardiovascular risk, such as serum cytokines or shortened leukocyte telomere length (LTL). Methods 170 patients with stable angina or troponin-positive acute coronary syndrome (ACS), referred for percutaneous coronary intervention (PCI) were prospectively enrolled and underwent full 3-vessel VH-IVUS pre-PCI. Troponin-I (cTnI), IL-6, IL-18, hsCRP, neopterin, MCP-1 and sICAM-1 were measured pre-PCI and 24-h post-PCI. LTL was determined by qPCR. The combined primary endpoint (MACE) included unplanned revascularisation, myocardial infarction (MI) and death, with a secondary endpoint of post-PCI MI (MI 4a). Results 18 MACE occurred in 16 patients (median follow-up: 625 (463–990) days). 30 372 mm of VH-IVUS were analysed and 1106 plaques classified (Abstract B Figure 1) locally and via a core-lab. After multivariable regression:Abstract B Figure 1 Total number of non-calcified VH-IVUS-identified thin capped fibroatheromata (VHTCFA) was the only factor independently associated with MACE (HR=3.16, (95%CI=1.16 to 8.64), p=0.025). Total VHTCFA number (OR=1.26 (1.03 to 1.53) p=0.021) and total stent length (OR=1.04 (1.01 to 1.08), p=0.01) were the only factors independently associated with MI 4a. A novel 3-vessel vulnerability index (necrotic core: fibrous tissue ratio) and side branch loss were independently associated with stenting-related cTnI rise (standardised beta coefficient (sβ)=0.29, p=0.004 and sβ=0.23, p=0.019 respectively). Necrotic core area at the minimum luminal area frame was the only factor independently associated with ACS presentation (OR=1.59, p=0.030). Stented vessel VHTCFA number (OR=1.75 (1.22 to 2.51), p=0.002) was independently associated with the lower LTL tertile (DNA-based cardiovascular risk predictor). Stenting-related IL-6 rise was the only biomarker independently associated with MACE (HR=1.03 (1.01–1.05), p=0.007). Conclusion We present the first report of an association between VHTCFA and MACE. This provides novel evidence that VHTCFA definitions are important in their own right (rather than as analogues of histological TFCA definitions). We also present the first report of associations between VHTCFA and MI 4a as well as a novel vulnerability index that is association with stenting-related troponin rise. Finally, we report a novel association between VHTCFA and DNA-based cardiovascular risk prediction (LTL).

7 GLP-1 cardioprotection is not mitochondrial K-ATP channel dependent

Introduction Glucagon-like Peptide-1 (GLP-1) protects against left ventricular (LV) stunning but the mechanism is unclear. Two protocols (P1 and P2) investigated whether blockade of mitochondrial K-ATP channels (responsible for ischaemic conditioning) with glibenclamide abrogates GLP-1 cardioprotection in humans. Methods P1. Patients attending for elective PCI to their LAD were assigned to 4 groups (Figure 1). Pressure-volume loops, allowing systolic/diastolic assessment, were recorded at baseline (BL1) and after 1-minute LAD balloon occlusion (BO1). GLP-1 or saline infusion was started after BO1, with loops repeated (BL2 and BO2) at 30mins. P2. Patients awaiting PCI underwent serial dobutamine stress echos (DSE) with tissue Doppler, to assess impact of GLP-1 and glibenclamide on global and regional systolic function. Results P1. BO1 reduced LV function in all groups. Recovery from stunning (BL2) and cumulative dysfunction (BO2) improved with GLP-1 alone, and when glibenclamide was added. P2. At peak stress and recovery there was additional improvement in systolic function with GLP-1 versus control. However, systolic function was unchanged, with and without glibenclamide. Conclusion Glibenclamide did not abrogate GLP-1-mediated cardioprotection, suggesting GLP-1 acts through a non-KATP-dependent pathway in humans. Abstract 7 Figure 1 Illustration of changes in systolic function over time in both protocols

16 Bioresorbable vascular scaffolds implanted for acute coronary syndrome are associated with reduced early strut coverage

Background Studies have suggested that neointimal growth and strut coverage is reduced in patients with acute coronary syndrome (ACS) receiving metallic stents. Use of more biocompatible devices such as bioresorbable vascular scaffolds (BVS) may facilitate early neointimal growth strut coverage. We aimed to assess whether neointimal growth is affected by clinical presentation, in a population undergoing BVS implantation. Methods BVS were implanted in patients for stable angina (SA) or ACS using optical coherence tomography (OCT) guidance. Repeat OCT was performed at follow-up (median 74 days), and BVS analysed at 1mm intervals for measures of scaffold/flow area, apposition, neointimal growth and strut coverage. Results 29 BVS were included (62% post ACS). There were no differences between procedural or lesion characteristics. Post-deployment, all BVS achieved >90% predicted scaffold area. Only 1.64% struts were incompletely apposed, compared to 0.47% at follow-up (p = 0.006). Reductions in mean scaffold (-4.0%, p = 0.01) and flow (-8.4%, p < 0.001) areas were observed at follow-up, with larger reductions in mean flow area for SA (-14.5 ± 14.2 vs. -4.9 ± 7.9%, p = 0.03). ACS led to reduced neointimal growth (0.51 ± 0.18 vs. 0.87 ± 0.37mm2, p = 0.002), and increased percentage of uncovered struts (2.68 ± 1.67 vs. 1.43 ± 0.87%, p = 0.015). Conclusions Neointimal growth and strut coverage is reduced following ACS in patients receiving BVS at an early timepoint, consistent with studies in metallic stents. This suggests use of more biocompatible devices may not improve early strut coverage.

045 PRIMARY PERCUTANEOUS CORONARY INTERVENTION FOR ST ELEVATION MYOCARDIAL INFARCTION: DOES DIRECT STENTING IMPACT ON MORTALITY?

Introduction Randomised trial data suggest that direct stenting (DS) during primary percutaneous coronary intervention (PPCI) for ST elevation myocardial infarction (STEMI) is associated with improved markers of reperfusion, such as ST segment resolution, myocardial blush grade and TIMI flow. However, there are few data as to whether these angiographic surrogates translate into a mortality benefit. Methods Consecutive patients attending two high-volume centres undergoing PPCI for STEMI between September 2008 and December 2010 were included in the analysis. All patients received aspirin 300 mg and clopidogrel 600 mg at point of STEMI diagnosis in the community. Use of predilatation (PD), manual thrombus aspiration (TA) and glycoprotein inhibitors (GPI) were at operator discretion. Demographic data and clinical outcomes were obtained by interrogation of local and national databases. Results A total of 1664 patients (mean age 65.3±12.5 years, 74.7% male) underwent PPCI during the study period. We excluded 77 who were not stented from the final analysis. Overall in hospital mortality was 3.0% (47/1587), with 30-day and 1-year mortality of 4.2% (66/1587) and 7.2% (114/1587) respectively. There was a significant 1-year survival advantage in patients who underwent DS (30.2%) compared with those who were stented after PD (3.16% vs 8.63%; p<0.001). GPI use was similar in both groups (57.7% DS vs 60.7% PD; p=0.29) whereas TA was higher in those who underwent DS (73.5% DS vs 61.1% PD; p<0.0001). However, in those patients who underwent DS, there was a trend towards greater mortality with TA (3.64% TA vs 1.83% no TA; p=0.35) suggesting that it is not the reason for mortality benefit in the DS group. Conclusion In an unselected real-world population undergoing PPCI for STEMI, DS is associated with a significant reduction in 1-year mortality. This effect appears to be independent of both GPI and TA use.

053 LONGTERM NATURAL HISTORY OF RADIOFREQUENCY INTRAVASCULAR ULTRASOUND IDENTIFIED CORONARY PLAQUES

Introduction Prior studies have shown that virtual-histology intravascular ultrasound (VH-IVUS) identified thin-capped fibroatheroma (VHTCFA) (figure 1) and plaque burden (PB) >70% are associated with major adverse cardiovascular events (MACE). This study examined non-culprit lesion features that predict MACE in long-term follow up and culprit lesion features responsible for myocardial infarction (MI). Table 1 Plaque characteristics Univariate analysis HR (95% CI) Univariate analysis p value Multivariate analysis HR (95% CI) Multivariate analysis p value VHThCFA 1.17 (0.23 to 6.24) 0.86 Total VHTFCA 6.37 (1.45 to 27.94) 0.014 2.18 (0.41 to 11.71) 0.36 Non-calcified VHTCFA 4.01 (0.87 to 18.68) 0.077 2.91 (0.57 to 15.00) 0.20 Calcified VHTCFA 1.51 (0.40 to 5.75) 0.55 Remodelling index 26.82 (0.36 to 1975) 0.13 MLA<4 mm2 3.61 (1.15 to 11.32) 0.028 1.23 (0.24 to 6.22) 0.80 Plaque burden>70% 7.77 (2.06 to 29.28) 0.002 7.77 (2.06 to 29.28) 0.002 Plaque volume (mm3) 1.00 (1.00 to 1.00) 0.34 Necrotic core volume (mm3) 1.00 (0.99 to 1.01) 0.57 NC percentage 1.01 (0.93 to 1.10) 0.79 Methods 170 patients with stable angina (n=100) or MI (n=70) underwent three-vessel VH-IVUS prior to percutaneous coronary intervention (PCI). Patients were followed for MACE which consisted of death, MI, cerebrovascular event, hospitalisation with unstable angina or unplanned revascularisation. Non-culprit lesion features were tested for association with future MACE, and culprit lesion features were assessed for initial presentation with MI, using univariate and multivariate analysis. Results 30 372 mm of VH-IVUS were analysed and 1096 plaques classified. 45 MACE occurred in 30 patients over a median follow up of 1115 (968–1537) days. These included 3 deaths, 6 MIs, 3 cerebrovascular events, 15 hospitalisations due to unstable angina, 3 unplanned coronary bypass operations and 15 unplanned PCI. By univariate analysis, non-culprit VHTCFA (HR=7.37, p=0.014), MLA<4 mm2 (HR=3.61, p=0.028) and PB>70% (HR=7.77, p<0.001) were associated with future non-restenotic MACE on long-term follow up (table 1). By multivariate analysis PB>70% (HR=7.77, p<0.001) remained independently associated with MACE. On univariate analysis, multiple culprit lesion features were associated with initial presentation with MI (table 2), including total and calcified VHTCFA, remodelling index, PB>70%, MLA <4 mm2, plaque rupture and thrombus. By multivariate analysis, PB>70% (OR (OR)=6.32, p<0.001), thrombus (OR=9.03, p<0.001) and MLA<4 mm2 (OR=3.01, p=0.02) were independently associated with MI. Interestingly, culprit lesion calcified VHTCFA were associated with initial MI (OR=2.59 (1.61–4.16), p<0.001), whereas non-calcified VHTCFA were more likely to be associated with future MACE HR=4.01 (0.87–18.68), p=0.077. Conclusion Despite the dynamic nature of coronary plaques, non-culprit VHTCFA, MLA<4 mm2 and PB>70% were associated with future MACE on long-term follow up, with PB>70% being independently associated. These same features in culprit lesions (amongst others) were associated with MI presentation, emphasising their biological importance. Interestingly, non-calcified VHTCFA are more likely to be associated with future MACE, whereas it is the calcified variant that is associated with MI presentation. This may represent a phenotypic transformation in the VHTCFA from non-calcified to calcified which could reflect multiple healed plaque rupture events (figure 2). This theory requires further investigation. Table 1 Non-culprit lesion features associated with future MACE VHThCFA (VH-IVUS thick-capped fibroatheroma), VHTCFA (VH-IVUS thin-capped fibroatheroma), MLA (minimum luminal area), NC (necrotic core), HR, CI Table 2 Plaque characteristics Univariate analysis OR (95% CI) Univariate analysis p value Multivariate analysis OR (95% CI) Multivariate analysis p value VHThCFA 0.84 (0.44 to 1.60) 0.59 Total VHTFCA 3.05 (1.78 to 5.23) <0.001 Non-calcified VHTCFA 1.18 (0.66 to 2.10) 0.58 Calcified VHTCFA 2.59 (1.61 to 4.16) <0.001 Remodelling index 28.05 (5.53 to 142.25) <0.001 MLA<4 mm2 8.86 (5.18 to 15.14) <0.001 3.01 (1.52 to 5.96) 0.002 Plaque burden>70% 15.41 (8.80 to 27.01) <0.001 6.32 (3.23 to 12.37) <0.001 Plaque volume (mm3) 1.004 (1.002 to 1.005) <0.001 Thrombus 20.29 (5.58 to 73.76) <0.001 9.03 (1.60 to 50.98) 0.013 Ruptured plaque 6.77 (2.09 to 21.92) 0.001 Table 2 Culprit lesion features associated with MI presentation OR Figure 1 VH-IVUS thin-capped fibroatheroma (VHTCFA). Figure 2 VH-IVUS thick-capped fibroatheroma (VHThCFA). Note that this fibroatheroma has two distinct layers (arrows) of necrotic core (red) and dense calcium (white), perhaps representing two temporally distinct plaque rupture events that have now healed.

060 CORONARY ROTATIONAL ATHERECTOMY USING BURR-TO-ARTERY RATIOS OF LESS THAN 0.5 IS ASSOCIATED WITH LOW LEVELS OF COMPLICATIONS, HIGH PROCEDURAL SUCCESS RATES AND FAVOURABLE 12-MONTH OUTCOMES

Background Rotational atherectomy (RA) is an established treatment of heavily-calcified coronary stenoses. Previous data suggest higher procedural complication rates when Burr-to-Artery (BTA) ratios exceed 0.7; the manufacturer-recommended BTA being 0.6. Little contemporary data exists regarding safe and optimal burr sizing, which may be important when considering RA via the radial approach with lower-caliber guiding catheters. Methods Single-centre retrospective review of patients undergoing elective RA between 2004 and 2011. Procedural success was defined as successful stent deployment with residual stenosis <30%, and complications defined as death, pericardial effusion/tamponade, coronary dissection/perforation and emergent CABG. Demographic and outcome data were obtained from local/national databases and casenote review. Quantitative coronary angiographic analysis was performed on archived films. Results Elective RA was successful in 197/220 cases (89.5%) with 72% of cases male and 22% diabetic (mean age 71.1±8.9 years). Target vessel was LAD (50.9%), RCA (35.0%), LCx (10.9%) and LMS (3.2%). Mean reference diameter was 3.45±0.6 mm and mean diameter stenosis (DS) 71.9±12.9%. Maximum burr size/case ranged from 1.25–2 mm (mode 1.5 mm) with mean BTA 0.43±0.08. 10 procedural complications occurred (4.5%); one wire fracture, two dissections, three perforations, two emergency CABG, one unretractable burr and one death. No difference in mean BTA was observed between procedures with/without complications (0.38±0.03 vs 0.43±0.08; p=0.33), but residual DS was higher in those with complications (12.3±21.2 vs 58.8±31.2; p<0.01). No correlation was observed between maximum burr size and age, sex, DS or minimum luminal diameter. At 36-month follow-up mortality was 11.7% and target vessel revascularisation (TVR) 22.8%. Conclusions Elective RA with low BTA is associated with high procedural success and low complication rates. These data imply that elective RA with a lower BTA than recommended is both safe and effective and need not preclude a transradial approach.

021 IS THERE A NEED FOR SPECIALIST CARDIAC CARE FOR PATIENTS WITH NON-ST ELEVATION MYOCARDIAL INFARCTION? AN ANALYSIS OF 85 780 PATIENT EPISODES FROM THE MINAP DATABASE 2008–2009

Background A previous analysis of the MINAP database in 2004/2005 indicated that patients admitted to hospital with myocardial infarction in England and Wales experienced better outcomes when cared for by specialist cardiology teams. Since then, routine care of ST-elevation myocardial infarction (STEMI) has been devolved wholly to cardiologists with the advent of primary PCI networks, and dissemination of clear guidance from NICE and the ESC for post-infarct patients that is readily available to all physicians has led to a move to downgrade/decommission coronary care units in some hospitals given a perceived lack of need. Table 1 Quartile Patients admitted to ACCU (% of nSTEMIs) Median length of stay (days, IQR) Access to coronary angiography (%) Crude 30-day mortality (%) Q1 ≤27% 7.5 (4.9–13.0) 56.2% 7.9% Q2 28–47% 6.8 (4.6–11.8) 52.1% 7.8% Q3 48–72% 6.5 (4.3–11.2) 58.6% 7.7% Q4 >72% 5.6 (3.6–9.6) 66.9% 5.6% Methods All patients presenting to hospitals in England and Wales 2008–2009 with non-STEMI (nSTEMI) recorded in the MINAP dataset (n=85 780) were included; outcomes analysed included access to specialist acute cardiac care units (ACCU; dedicated coronary care units or cardiology wards) and coronary angiography, provision of secondary preventative medications, length of hospital stay and mortality. Results 47% of nSTEMI cases (39 674/85 780) were admitted under specialist cardiology care compared with 36% in 2004–2005. When hospitals were divided by proportion of nSTEMI admissions to ACCU, access to coronary angiography was higher and median length of stay lower incrementally by quartile (table). When adjusted for confounding variables (age, sex, relevant comorbidities), relative risk of hospital stay less than overall median compared with Q1 was: Q2 1.21 (95% CI 1.8 to 1.3), Q3 1.32 (95% CI 1.3 to 1.4) and Q4 1.62 (95% CI 1.6 to 1.7; all comparisons p<0.001). Prescription of appropriate secondary preventative medications was better for patients admitted to ACCU (ORs: aspirin 1.56, 95% CI 1.2 to 2.0, p<0.001; β-blocker 1.21, 95% CI 1.1 to 1.4, p<0.005; ACE inhibitor 1.36, 95% CI 1.2 to 1.5, p<0.0001; statin 1.23, 95% CI 1.0 to 1.5, p<0.05) with the exception of clopidogrel, which was similar (OR 1.11, 95% CI 0.9 to 1.3, p=0.1). Unadjusted crude mortality was lowest for hospitals admitting the highest proportion of patients to ACCU (table). Relative risk of death within 30 days after adjustment for confounding variables for patients admitted with nSTEMI to ACCU compared with general medical facilities was 0.88 (95% CI 0.8 to 0.9; p<0.001). Conclusions Despite improved care for patients with STEMI in England and Wales, the need for specialist cardiac care for patients with nSTEMI is mandated in terms of economy (length of stay), quality of care (medication provision) and clinical governance (mortality). Patients with nSTEMI should therefore universally be admitted under the care of cardiologists, in expanded ACCU facilities.

026 Left bundle branch block as an activation criterion for primary percutaneous coronary intervention: where is the evidence?

Background The activation criteria for primary percutaneous coronary intervention (PPCI) includes chest pain in association with either ST-segment elevation (STEMI) or new-onset left bundle branch block (LBBB) on the ECG. However, defining LBBB as new is challenging acutely and the poor specificity of indeterminate chronicity LBBB may result in unnecessary PPCI activations. Published data are conflicting with regard to the utility of LBBB as a triage criterion for PPCI and subsequent outcomes are undefined. Methods Consecutive patients attending a single UK tertiary centre for presumed PPCI between September 2008 and December 2010 were included (n=1328). The activation ECG was obtained from the hospital PPCI database, as were demographic data. Outcome data were obtained from notes and national databases. MACE was defined as a composite of mortality and unplanned revascularisation. Two interventionists blinded to patient outcome reviewed the angiographic images and adjudicated if the activation was appropriate. Results Chest pain with LBBB (LBBB-activation) occurred in 88 patients (6.6%) of the PPCI cohort. Comparing LBBB-activations to those with STEMI demonstrated that LBBB-activations were older (mean age 70.3±12.4 vs 64.6±13.4 years; p<0.001) and less likely to be male (67.0% vs 76.8%; p=0.004). Otherwise, baseline demographics were similar. Eighteen (20.5%) patients with LBBB had an acute thrombotic coronary occlusion confirmed at angiography and received PPCI. The final adjudicated diagnoses for LBBB-activations were acute coronary syndrome (ACS) (39.8%), non-ACS cardiac (28.4%) and non-cardiac (31.8%). A history of previous MI (p=0.002) and presence of cardiogenic shock on arrival (p=0.04) were more prevalent in the appropriate LBBB-activations. One-year mortality and MACE were higher for appropriate LBBB-activations than the STEMI activations (27.8% vs 7.9%; p=0.002 (Abstract 026 figure 1) and 33.3% vs 9.1%; p<0.001 respectively).Abstract 026 Figure 1 Conclusions Less than half of LBBB-activations had an ACS and, of these, only half had a thrombotic coronary occlusion requiring PPCI. However, LBBB-activations have a significantly worse prognosis and merit urgent referral. Enhanced triage methods are required to correctly identify acute MI requiring PPCI in those with LBBB.Abstract 026 Figure 2

43 Prognosis after primary percutaneous coronary intervention for stemi: can the syntax score help?

Background Factors affecting prognosis after primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction (STEMI) include age at presentation, the presence of diabetes mellitus, left ventricular function and/or cardiogenic shock. Although the debate continues over a strategy of complete revascularisation (immediate or staged) vs culprit-only, little is known about the impact of the extent of coronary disease at presentation on prognosis after PPCI. The SYNTAX score, designed to stratify outcomes in multivessel PCI and CABG, has been validated in unselected populations undergoing elective PCI; to date, no studies have assessed its utility in PPCI. Methods Consecutive patients attending a single UK tertiary centre for PPCI between September 2008 and June 2010 (n=695) were included. SYNTAX scoring was performed by a single trained operator blinded to patient details and outcome. Scoring was validated by analysis of 3 separate cohorts by 2 other experienced operators. Patients were split into 3 subgroups as in the SYNTAX trial (score ≤22 (low, L), 22.5–32 (intermediate, IM) and ≥32.5 (high, H)), and patient data and outcome measures obtained by interrogation of local and national databases. Results 671 of 695 patients were included in the analysis with 24 being excluded owing to inability to score (previous CABG, images unavailable). The ability to allocate a SYNTAX tertile was reproducible between observers (r=0.94). Median scores in the 3 groups were: L 14, IM 26, H 36 (Abstract 43 figure 1A). Although there was no correlation between SYNTAX score and patient sex or diabetic status, there was a linear relationship with patient age (r2=0.03; p<0.0001). 1-year absolute survival (Abstract 43 figure 1B) followed SYNTAX score groups: L 94.7%, IM 88.7%, H 82.1% (p=0.0002). Similar results were obtained for freedom from death or unplanned revascularisation (p<0.0001) and death or any revascularisation (p<0.0001).Abstract 43 Figure 1 Conclusions The SYNTAX score, when applied to an unselected population of patients undergoing PPCI for STEMI, provides important prognostic information regarding 1-year survival from death and revascularisation. These findings may provide supporting evidence towards routine complete revascularisation of obstructive coronary artery disease after PPCI.

107 Plaque composition and plaque volume in non-stented vessels determines serum biomarker levels after stenting in stable angina: a VH-IVUS study

Introduction Previous work has shown that plaque composition in stented vessels determined by virtual histology intravascular ultrasound (VH-IVUS) predicts myocardial necrosis after percutaneous coronary intervention (PCI). However, disease in non-stented vessels may also determine myocardial necrosis, for example, reduced collateral blood flow may increase the area of myocardial necrosis after PCI. We examined whether plaque composition or volume (determined by VH-IVUS) in non-stented vessels or the whole coronary tree contributed to stenting-related rises in serum biomarkers. Methods Hundred patients with stable angina, referred for elective PCI underwent full 3-vessel VH-IVUS. Serum Troponin-I, interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hsCRP) were measured before and 24 h after PCI. Troponin-I and hsCRP results were logarithmically transformed (log10) to a normal distribution to permit calculation of Pearsons correlation coefficient. Results In stable angina patients, there was no significant difference in total plaque volume (563±60 mm3 vs 632±62 mm3 respectively, mean±SEM p=0.42), nor in necrotic core volume (NC) (73±13 mm3 vs 61±10 mm3 respectively, p=0.48) between stented and non-stented vessels. After PCI for stable angina the biomarker levels were: troponin-I: 0.27 ng/ml (0.06–0.94 ng/ml), IL-6: 8.0 pg/ml (5.5–11.4 pg/ml) and hsCRP: 5.7 mg/l (3.4–10.0 mg/l) (median (IQR)). Troponin-I levels correlated with total NC and total plaque volume on 3-vessel VH-IVUS (r=0.45, p=0.003; r=0.417, p=0.006 respectively), and in non-stented vessels (NC vs troponin-I: r=0.423, p=0.006; plaque volume vs troponin-I: r=0.37, p=0.018). However there was no correlation between troponin-I and either NC or plaque volume in the stented vessels (p=0.2 and p=0.45 respectively). Similarly, serum IL-6 correlated with both NC and plaque volume on 3-vessel VH-IVUS (r=0.414, p=0.009; r=0.412, p=0.009 respectively) and in non-stented vessels (r=0.47, p=0.003; r=0.376, p=0.003 respectively). However, there was no correlation between IL-6 and NC or plaque volume in stented vessels (p=0.33 and p=0.47 respectively). There were no significant correlations between VH-IVUS parameters and hsCRP. Adjusting for plaque volume the correlation between the 3-vessel NC/total plaque volume ratio and IL-6 remained (r=0.329, p=0.044) but not between 3-vessel NC/plaque volume ratio and troponin-I (p=0.23). Although Troponin-I rise correlated with total length of stents implanted (r=0.36, p=0.002), IL-6 and hsCRP did not (p=0.41 and p=0.94 respectively). Conclusion Three-vessel and non-stented vessel plaque composition and plaque volume determined by VH-IVUS correlate with troponin-I and IL-6 levels after PCI for stable angina, whereas plaque composition or plaque volume of the stented vessel do not. This difference highlights the importance of disease in non-stented vessels in PCI-related myocardial necrosis.